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PubMed1977

Calcium antagonism of the block in excitation-contraction coupling produced by a urea exposure-removal treatment.

Exposing frog's toe muscles to Ringer's solution made hypertonic with 400 mM urea for 60 min followed by placing the muscles back in Ringer's (urea-removal treatment) completely blocks the twitch without disrupting the surface openings of the T-tubules. The urea-removal treatment also increased the triadic junction width. Placing the muscles in Ringer's with an elevated calcium concentration (5 mM) following exposure to the hyertonic solution prevented the block of the twitch response but not the increase in the triadic junction width. Exposing untreated muscles to Ringer's with 5 mM calcium either had no effect on the twitch on reduced it by 30 percent or less. These results suggest the possibility that increasing the width of the triadic junction decreases the amount of calcium ions reaching the terminal cisternae during an action potential thereby blocking the twitch. Elevating the calcium concentration in the T-tubules would increase the amount of calcium which enters the triadic junction during an action potential and thus antagonize the above effects.

Action Potentials↗
PubMed1993

Persistent mechanical effects of decreasing length during isometric contraction of ovarian ligament smooth muscle.

When isometrically-contracting strips of ovarian ligament smooth muscle were suddenly shortened by 10-20% of their length, force fell rapidly and then redeveloped along an exponential time course. The amount of force recovered fell short of that expected in an isometric contraction at the new length, and this force deficit was proportional to the magnitude of the length step (approximately 80% of force was recovered after a 10% shortening). A sudden imposed decrease in length was more effective in reducing subsequent force than was isotonic shortening. Early in the recovery phase the stiffness of the muscle was decreased to less than its expected value; stiffness recovered to expected levels on an exponential time course approximately three to four times faster than force recovery itself. Force-velocity curves made during the redevelopment phase showed a reduced maximal force (Fmax) and an increased maximal shortening velocity (Vmax) when compared with control contractions matched in force, time and length. The curves crossed at approximately 10% of Fmax. During isometric relaxation the muscles showed an increase in their expected stiffness; prior imposed shortening (as above) reduced the relaxation stiffness increase in proportion to the prior force deficit. The persistent effects of early events on the later phases of the contraction, as well as the increase in shortening velocity with very light loads, are consistent with the hypothesis that the sudden shortening detaches crossbridges and that same fail to reattach during force recovery. During isotonic shortening of unperturbed muscle some slowly-cycling crossbridges may act as an internal load and reduce shortening velocity.

Animals↗
PubMedDate not supplied

Neurophysiologic inhibition of strength following tactile stimulation of the skin.

A modified shoulder abduction manual muscle test was incorporated in this study to demonstrate strength changes following tactile stimulation of the skin. Resistance was applied to the distal radioulnar joint and the stimulus (scratching) was applied inferior to the clavicle on the clavicular head of the pectoralis major muscle after maximum contraction. An electromechanical device quantified the isotonic (eccentric) measurements. A standard dynamometer system (Cybex II) was used to measure isometric strength. The nondominant side was used as the "control." Two populations, a normal (random) and a strong (athletic) group, were studied. Twenty-three persons (52% women, 48% men; mean age, 27 years; mean height, 67 inches (170 cm); and mean weight, 147 lb (66.7 kg)) were in the "normal" group and 17 persons (100% men; mean age, 25 years; mean height, 74 inches (188 cm); and mean weight, 215 lb (97.5kg)) were in the "strong" group. The random population showed a 19% decrease in strength following tactile stimulation as measured by the manual muscle testing unit; the athletic population showed a 17% decrease in strength. With the isometric measurements, the random population had an 8% decrease in mean strength following the scratch but the athletic population showed no significant decrease. The capability to quantify objectively manual muscle tests is discussed in relation to the importance of the proximal musculature.

Adult↗
PubMed1983

Biomechanical considerations in the modeling of muscle function.

The instantaneous functional role of a voluntary muscle in the neighborhood of a joint is often described in clinical terms (e.g. flexor; abductor; external rotator; agonist; contracting concentrically and isokinetically) that seen sufficiently explicit and clear in certain simple situations, but have not yet been carefully defined in precise biomechanical terminology for the general case. In order to describe the functional role of a voluntary muscle as its acts to change and/or maintain the configuration of a joint, it is necessary to make certain modeling assumptions. These include modeling the joint, modeling the muscle force line of action in the joint neighborhood, and establishing the location and orientation of the three joint axes for all possible joint configurations. Modeling the joint as a point leads to simple and sensible definitions which are consistent with clinical practice. The straight line model is most conveniently used to establish the muscle force line of action. A RHO coordinate system embedded in the distal joint segment with origin at the joint center point, and with intersecting axes coincident with the F/E, A/A and I/XR axes when the joint is in the anatomical position, is the joint coordinate system of choice to describe the turning effects of the muscle about the joint. Sensible and simple biomechanical definitions for clinical terms describing muscular contractions (i.e. concentric; eccentric; isometric; isokinetic; isotonic) were presented and appear to be relatively uncontroversial. Alternative biomechanical definitions for agonistic and antagonistic muscular activity were also presented, as were arguments for choosing a simple definition based on using the joint resultant moment as the criterion measure relative to which the individual muscle's moment about J should be compared. Biomechanical definitions for determining when a muscle functions as a joint flexor or extensor, abductor or adductor, and internal or external rotator were also presented. These definitions were based on the classical concept where the muscle's instantaneous turning effect is determined by its moment about the joint center. The algebraic signs and relative magnitudes of the components of the muscle's moment about J were used to determine not only the functional behavior of the muscle (e.g. flexor vs. extensor), but also the relative contributions of the muscle to producing rotations about the three joint axes through J. A detailed critique of the restricted functional classification scheme proposed by Molbech and Carlsöö was also presented.(ABSTRACT TRUNCATED AT 400 WORDS)

Biomechanical Phenomena↗
PubMed1988

[Experimental study on interdigestive migrating contractions with intestinal transection and injection of Ringer solution into intestine].

The occurrence and mechanism of IMC are still not completely elucidated. Base on the conjecture of that the region of intestine and its ingredients may be concerning with the conduction mechanism of IMC, following experiment was performed by author. Small intestine was cut into two parts. Anal side was closed as blind end, and the end of oral side was sutured to colon or anal part of intestine by end to side anastomosis. Gastric fistula and intestinal fistula of the blind ending intestine were also made, and six pieces of force transducers were sutured to the serosa of the intestine in order to observe the movement of intestine. Under non-anesthesia and non-restricted condition for whole day long, Ringer solution was injected into gastric or intestinal fistula by 50 ml one shot or continuous dripped infusion of 250 ml per hour. The result is: In upper part of intestine, the appearance of IMC in oral and anal side of intestine is continuously observed. However, in lower part of intestine, the IMC of oral and anal part of intestine appeared completely independent without any continuity. And, as one shot of 50 ml of Ringer solution was injected, the conduction of IMC was suppressed but still observable, while continuously infused of 250 ml/hr, the IMC was completely disappeared.

Anastomosis, Roux-en-Y↗
PubMed1991

High potassium contents in organ preservation solutions cause strong pulmonary vasocontraction.

Euro-Collins (ECS) and UCLA-formula organ preservation solutions induced strong vasocontraction in porcine pulmonary arteries when studied in organ baths at temperatures of 37 degrees C and 30 degrees C. At 20 degrees C ECS induced a 30% contraction, but at 6 degrees C no contraction (n = 5) or a weak contraction (n = 1) was elicited. Neither prostaglandin E1 nor nifedipine caused any significant reduction of the vasocontraction elicited by ECS and UCLA. Krebs solution, enriched with potassium in amounts corresponding to those in ECS (115 mmol/L) or UCLA (30 mmol/L), induced vasocontraction comparing well with those induced by ECS or UCLA, indicating that it is the high potassium content that causes the vasocontraction. In a second experiment lung segments were stored at 4 degrees C for 9 hours in ECS, UCLA, or Krebs solution. Pulmonary arterial segments were then studied in organ baths at 37 degrees C. The choice of preservation solution did not significantly affect the contractile properties of potassium, noradrenaline, or the thromboxane mimic U-46619. To conclude, high potassium contents in organ preservation solutions induce strong pulmonary vasocontraction in lung temperatures greater than 20 degrees C but not in temperatures less than 10 degrees C. These vasocontractions are not significantly reduced by prostaglandin E1 or nifedipine. We suggest that the initial preservation solution used to cool down the lungs should contain 4 mmol/L or no potassium. When the lung temperature is less than 10 degrees C, a second perfusion might be done, and then a high potassium content (if thought to be essential) will not cause vasocontraction.

Alprostadil↗
PubMed1999

[Role of the Na+/H+ pump in heart ischemia-reperfusion lesions in the neonatal period].

OBJECTIVE: Amiloride 5-(N,N-dimethyl)(AMD), an Na+/H+ pump inhibitor, was used to evaluate the maturity and sensitivity of the Na+/H+ pump in neonatal myocardial cells. METHOD: Using the isolated contraction isometric heart model, the hearts of neonatal rabbits (10-12 days) were stopped by cardioplegia with and without AMD (20 mumoles/l), then submitted to 40 minutes of ischaemia at 37 degrees C or 120 minutes of ischaemia at 20 degrees C before being reperfused for 30 minutes at 37 degrees C. When AMD was added to the cardioplegic solution, it was also added (20 mumoles/l) to the Krebs solution for the first five minutes of reperfusion. Functional assessment of myocardial contractility and relaxation was performed before aortic clamping and after 30 minutes of reperfusion. Coronary venous drainage during reperfusion was collected to evaluate CPK levels. RESULTS: To 37 degrees C or 20 degrees C, Na+/H+ pump inhibition was marked by improvement of all myocardial contractility and relaxation parameters at the end of the reperfusion period. A significantly reduced CPK release wase also observed during reperfusion associated with Na+/H+ pump inhibition. CONCLUSION: This study demonstrates maturation of the Na+/H+ pump in neonatal myocardial cells and confirms the role of this ion exchange pump in the pathogenesis of ischaemia-reperfusion lesions. The study at 20 degrees C demonstrated the sensitivity of the Na+/H+ pump to a low transmembrane proton gradient.

Age Factors↗
PubMed1996

Initial reperfusion with 2,3 butanedione monoxime is better than hyperkalemic reperfusion after cardioplegic arrest in isolated guinea pig hearts.

OBJECTIVE: Initial warm cardioplegic reperfusion is widely used to ameliorate cardiac reperfusion damage after cardioplegic arrest. However, undesired effects of the high potassium concentration of the cardioplegic perfusate may limit the beneficial effect of this treatment. Contraction uncoupling by a negative inotropic and vasodilating agent such as 2,3-butanedione monoxime (BDM) may be superior to warm cardioplegic reperfusion in reducing reperfusion damage. Thus, initial reperfusion with BDM was compared with hyperkalemic reperfusion (HKR) after global ischemia of Langendorff-perfused guinea pig hearts. METHODS: Cardiac arrest was induced in 16 hearts using hyperkalemic Krebs' solution and hearts were stored unperfused at 37 degrees C for 40 min. Two groups were studied: HKR, initial reperfusion with 37 degrees C oxygenated hyperkalemic Krebs' for 5 min, and BDM, addition of 20 mM BDM to normokalemic Krebs' for 5 min. RESULTS: BDM increased reactive coronary reflow (128 +/- 8%; all data mean +/- SEM of baseline) much more than HKR treatment (65 +/- 5%). O2 consumption was reduced more by HKR (28 +/- 1%) than by BDM (42 +/- 4%), but the O2 supply/consumption ratio was higher with BDM. During perfusion with normal Krebs' solution, flow stabilized at about 75% of baseline in both groups. Post-ischemic responses to adenosine, serotonin, and nitroprusside were depressed to a similar degree in both two groups. Recovery of left ventricular developed pressure was better in BDM (69 +/- 2%) than in HKR (61 +/- 3%)-treated hearts. Reperfusion dysrhythmias were markedly reduced after BDM reperfusion. CONCLUSIONS: These data indicate that treatment in the initial 5-min reperfusion period with BDM is more effective than hyperkalemic reperfusion in reducing reperfusion damage.

Animals↗
PubMed1999

Contractions in human detrusor smooth muscle induced by hypo-osmolar solutions.

PURPOSE: The aim of this study was to investigate stretch activated channels in human detrusor using hypo-osmolar solutions to produce cell deformation. Stretch activated channels could provide another mechanism by which detrusor myocytes may be coupled. MATERIALS AND METHODS: Human detrusor removed at surgery was dissected into strips and also enzymatically digested and cultured. Strips (5x1x1 mm.) were mounted in an organ bath and perfused with gassed Tyrode's. Hypo-osmolar solutions were made by removal of NaCl. Gadolinium (Gd3+), a blocker of stretch activated channels (SACs), and diltiazem, an L-type Ca2+ channel antagonist were used at 10 microM concentrations. Mean data +/- S.E.M. are expressed as a percentage of maximal tension produced by 1 microM carbachol for each patient. Enzymatically disaggregated, human detrusor was cultured in flasks, passaged and placed on glass coverslips. Once confluent the cells were incubated with the Ca2+ sensitive fluorochrome Fura-2AM. Coverslips were placed in a bath on the stage of EPI-fluorescence microscope and solutions were perfused through the bath (5 ml. per minute, 35C, pH 7.4). Changes in fluorescence emission ratio (proportional to changes in cytosolic Ca2+) were measured. RESULTS: Hypo-osmolar solutions produced a tension increase in the strips and a Ca2+ influx in the cells. In the strips in paired experiments Gd3+ and diltiazem significantly reduced the response to hypo-osmolar solution (87%+/-16% v. 51%+/-12.5%, p = 0.003, n = 10 for Gd3+), and (69%+/-11% v. 37%+/-9%, p = 0.001, n = 9 for diltiazem). In Ca2+ free solution responses were significantly reduced (65%+/-10% v. 21%+/-8%, p = 0.001, n = 9). In the cells in paired experiments, 10 microM Gd3+ significantly reduced the elevation of cytosolic Ca2+ in response to hypo-osmolar solutions (median 0 v. 0.38 (62 cells, n = 7 bladders)), as did Ca2+ free hypo-osmolar solution (median 0 v. 0.44 (46 cells, n = 7)). 10 microM diltiazem (L-type Ca2+ channel antagonist) did not influence the response to hypo-osmolar solution (p = 0.14, median 0.5 v. 0.54 (31 cells, n = 4)). CONCLUSIONS: Hypo-osmolar solutions produced a tension increase in human detrusor that appears to be dependent on upon influx of Ca2+ through stretch activated channels (SACs), influx of Ca2+ through L-type Ca2+ channels and also on release of intracellular Ca2+.

Calcium Channel Blockers↗
PubMed1979

The effects of temperature on the energetics of rat papillary muscle.

The mechanical and myothermic responses of left ventricular papillary muscles from adult rats have been examined at 20 degrees and at 27 degrees C. Contraction trains of six isometric or isotonic twitches at 1/6 Hz were used to establish the heat-stress and load-enthalpy relations respectively. Peak isometric stress was slightly higher at 20 degrees than at 27 degrees C (45 vs. 41 mN/mm2) and was inversely related to muscle cross-sectional area. The stress-independent heat component, identified with the activation heat, was 75% greater at the lower temperature. The stress-dependent heat component, identified with the heat of actin-myosin interaction, was unaffected by temperature. In isotonic experiments the external work performance was similar at both temperatures but the heat liberation was significantly enhanced at the lower temperature so that mechanical efficiency (external work/enthalpy) was reduced. Evidence is presented suggesting that the preparations were not O2-diffusion limited at either temperature. The results are discussed in terms of known functional anomalies of rat cardiac tissue.

Animals↗
PubMed1994

Effects of adenosine on Ca2+ transients and tension in aequorin-injected ferret papillary muscles.

The effects of adenosine on Ca2+ transients and tension in ferret papillary muscles were investigated using the aequorin method. Adenosine (0.01-1 mM) reduced the peak of Ca2+ transients and caused a slight concentration-dependent decrease in tension. Adenosine prolonged the decay time of Ca2+ transients but did not alter the time course of tension. In isoproterenol (0.1 microM)-treated preparations, adenosine decreased the peak of Ca2+ transients but did not alter the peak of tension. Adenosine prolonged the isoproterenol-shortened decay time of Ca2+ transients. The effects of adenosine on Ca2+ transients were antagonized by the selective A1 receptor antagonist 8-cyclopentyl-1,3,-dipropylxanthine. In the presence of isoproterenol, adenosine (0.1 mM) shifted the intracellular [Ca2+]/tension relation to the left. These results can be explained by the hypothesis that adenosine inhibits the activity of adenylate cyclase via stimulation of the A1 receptor, other mechanisms however cannot be overlooked. The prolongation of the decay time of Ca2+ transients and the increase in the Ca2+ sensitivity of the contractile elements are the underlying mechanisms of adenosine which maintain developed tension in twitch response, although adenosine decreases the peak of Ca2+ transients.

Adenosine↗
PubMed1994

Coronary reserve and contractile reserve in crystalloid- and blood-perfused rabbit hearts.

Coronary reserve and contractile reserve were compared between crystalloid-perfused and blood-perfused rabbit hearts at various perfusion pressures (40-110 mmHg). Contractile function of the crystalloid-perfused hearts was dependent on the perfusion pressure, according to Gregg's phenomenon. Developed left ventricular pressure (LVP) increased from 67 +/- 6 mmHg to 121 +/- 5 mmHg and positive dP/dt maximum (dP/dt max) from 1,083 +/- 75 to 2,233 +/- 126 mmHg/s at perfusion pressures between the lowest and highest perfusion pressure. In the blood-perfused hearts, the perfusion pressure-induced changes were less pronounced: developed LVP changed from 107 +/- 11 mmHg to 138 +/- 8 mmHg and dP/dt max from 1,517 +/- 181 to 2,008 +/- 187 mmHg/s. The blood-perfused hearts showed better cardiac function, especially negative dP/dt minimum (dP/dt min), compared to the crystalloid-perfused hearts. Contractile reserve estimated by paired pacing technique was quite independent of the perfusion pressure in the blood-perfused hearts but not in the crystalloid-perfused hearts, and was significantly better in the blood-perfused hearts (e.g., 81% increase of developed LVP with blood perfusion, and 26% increase with crystalloid perfusion at a perfusion pressure of 80 mmHg). Coronary reserve, estimated by reactive hyperemia, was independent of the perfusion pressure in both groups. Coronary reserve was small in the crystalloid-perfused hearts (< 23%) and more than double the control value in the blood-perfused hearts. It is proposed that blood-perfused hearts are more suitable for physiological and pathophysiological studies.

Animals↗
PubMed1999

Total Ca handling in canine mild Ca overload failing heart.

We analyzed total Ca handling of the left ventricle (LV) in the mildly failing heart preparation induced by a temporary intracoronary Ca overloading intervention in eight excised and cross-circulated canine hearts. This Ca intervention consisted of interruption of coronary blood perfusion by Ca-free oxygenated Tyrode perfusion for 10 min followed by high-Ca (16mmol/l) oxygenated Tyrode perfusion for 5 min. This intervention decreased the LV contractility index, Emax (end-systolic maximum elastance), by 40% after restoration of the blood cross-circulation. We expected a Ca overload or paradox failing heart resembling the postischemic stunned heart and being characterized by an increased O2 cost of Emax. However, LV O2 consumption under mechanically unloading conditions decreased by 30% from control without increasing the O2 cost of Emax. To obtain a mechanistic view of this failing heart, we investigated cardiac total Ca handling by our integrative analysis method. In this method, we obtained the internal Ca recirculation fraction (RF) from the decay beat constant of the postextrasystolic potentiation following each sporadic spontaneous extrasystole in these failing LVs. We combined the RF with the decreased Emax and the unchanged O2 cost of Emax in our recently developed formula of total Ca handling. We found that these failing LVs had a slightly but significantly increased RF accompanied by either a slightly increased futile Ca cycling or a slightly decreased Ca reactivity of Emax, or both. Any of these three possible changes can account for the unchanged O2 cost of Emax. This result indicates that the present mildly failing heart has not yet fallen into a typical Ca overload or paradox by the temporary Ca overloading intervention.

Animals↗